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001-es BibID:	BIBFORM050560
Első szerző:	Mistry, Shilpa
Cím:	Prolonged exposure to bradykinin and prostaglandin E2 increases TRPV1 mRNA but does not alter TRPV1 and TRPV1b protein expression in cultured rat primary sensory neurons / Shilpa Mistry, Cleoper C. Paule, Angelika Varga, Andy Photiou, Agnes Jenes, Antonio Avelino, Laki Buluwela, Istvan Nagy
Dátum:	2014
ISSN:	0304-3940
Megjegyzések:	Sensitisation of the capsaicin receptor, transient receptor potential vanilloid type 1 (TRPV1) ion channel in nociceptive primary sensory neurons (PSN) underlies the development of inflammatory heat hyperalgesia. Removal of the negative-dominant splice variant of the TRPV1 molecule, TRPV1b from TRPV1/TRPV1b heterotetrameric channels, which should be associated with changes in the expression of TRPV1 and TRPV1b transcripts and proteins, has been suggested to contribute to that sensitisation. Respective reverse-transcriptase polymerase chain reaction (RT-PCR) and Western-blotting revealed that both TRPV1 and TRPV1b mRNA, and their encoded proteins are expressed in rat cultured PSN. Sequencing of the RT-PCR products showed that TRPV1b mRNA lacks the entire exon 7. Further, growing PSN for 2 days in the presence of 10műM bradykinin (BK) and 10műM prostaglandin E2 (PGE2) significantly increases TRPV1 responsiveness and TRPV1 mRNA expression, without producing any changes in TRPV1b mRNA, and TRPV1 and TRPV1b protein expression. These data challenge the hypothesis that alterations in the composition of the TRPV1 ion channel contributes to the sensitisation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Neuroscience Letters. - 564 (2014), p. 89-93. -
További szerzők:	Paule, Cleoper C. Varga Angelika (1977-) (biológus) Photiou, Andy Jenes Ágnes (1980-) (élettanász) Avelino, Antonio Buluwela, Laki Nagy István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM050561
035-os BibID:	PMID:24114173
Első szerző:	Varga Angelika (biológus)
Cím:	Anandamide produced by Ca2+-insensitive enzymes induces excitation in primary sensory neurons / Angelika Varga, Agnes Jenes, Timothy H. Marczylo, Joao Sousa-Valente, Jie Chen, Jonothan Austin, Srikumaran Selvarajah, Fabiana Piscitelli, Anna P. Andreou, Anthony H. Taylor, Fiona Kyle, Mohammed Yaqoob, Sue Brain, John P. M. White, Laszlo Csernoch, Vincenzo Di Marzo, Laki Buluwela, Istvan Nagy
Dátum:	2014
ISSN:	0031-6768
Megjegyzések:	The endogenous lipid agent N-arachidonoylethanolamine (anandamide), among other effects, has been shown to be involved in nociceptive processing both in the central and peripheral nervous systems. Anandamide is thought to be synthesised by several enzymatic pathways both in a Ca2+-sensitive and Ca2+-insensitive manner, and rat primary sensory neurons produce anandamide. Here, we show for the first time, that cultured rat primary sensory neurons express at least four of the five known Ca2+-insensitive enzymes implicated in the synthesis of anandamide, and that application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl, the common substrate of the anandamide-synthesising pathways, results in anandamide production which is not changed by the removal of extracellular Ca2+. We also show that anandamide, which has been synthesised in primary sensory neurons following the application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl induces a transient receptor potential vanilloid type 1 ion channel-mediated excitatory effect that is not inhibited by concomitant activation of the cannabinoid type 1 receptor. Finally, we show that sub-populations of transient receptor potential vanilloid type 1 ion channel-expressing primary sensory neurons also express some of the putative Ca2+-insensitive anandamide-synthesising enzymes. Together, these findings indicate that anandamide synthesised by primary sensory neuron via a Ca2+-insensitive manner has an excitatory rather than an inhibitory role in primary sensory neurons and that excitation is mediated predominantly through autocrine signalling. Regulation of the activity of the Ca2+-insensitive anandamide-synthesising enzymes in these neurons may be capable of regulating the activity of these cells, with potential relevance to controlling nociceptive processing.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Pflugers Archiv. - 466 : 7 (2014), p. 1421-1435. -
További szerzők:	Jenes Ágnes (1980-) (élettanász) Marczylo, Timothy H. Sousa-Valente, Joao Chen, Jie Austin, Jonothan Selvarajah, Srikumaran Piscitelli, Fabiana Andreou, Anna P. Taylor, Anthony H. Kyle, Fiona Yaqoob, Mohammed Brain, Sue White, John P. M. Csernoch László (1961-) (élettanász) Di Marzo, Vincenzo Buluwela, Laki Nagy István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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